Pub Date : 2021-12-04DOI: 10.15586/qas.v13isp1.1009
Amin Mousavi Khaneghah
Quality, safety, and nutrient values of food products can be changed under various conditions along the production chain, even on consumers’ tables. Although based on the scientific reports, many techniques, including conventional and emerging technologies, are approached during harvest, post-harvest, processing, storage, and distribution of food products, the idea of minimal processing of food products still attracted considerable attention.
{"title":"New emerging techniques in combination with conventional methods in improving the quality, safety, and nutrient values of food products","authors":"Amin Mousavi Khaneghah","doi":"10.15586/qas.v13isp1.1009","DOIUrl":"https://doi.org/10.15586/qas.v13isp1.1009","url":null,"abstract":"Quality, safety, and nutrient values of food products can be changed under various conditions along the production chain, even on consumers’ tables. Although based on the scientific reports, many techniques, including conventional and emerging technologies, are approached during harvest, post-harvest, processing, storage, and distribution of food products, the idea of minimal processing of food products still attracted considerable attention.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42572149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Psoriasis is a common chronic, inflammatory skin disease possessing properties of inflammatory cell infiltration and excessive proliferation of keratinocytes, the occurrence and development of which remain fully elucidated. Therefore, the study was designed to determine the effects of kirenol (50, 100 and 200 μg/mL) on Cultured Human Keratinocytes (cells) (HaCaT) in vitro and reveal its molecular mechanism. The in vitro psoriasis model was established utilizing tumor necrosis factor-α (TNF-α)-stimulated HaCaT cells. Kirenol, a diterpenoid compound, was applied at different concentrations (50, 100 and 200 μg/mL) to HaCaT cells for 24 h. The Cell Counting Kit-8 (CCK-8) and thymidine monobromodeoxyuridine (BrdU) assays were used to assess cell viability and proliferation, followed by assessment of cell migration by Transwell assay. Subsequently, inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA), and Western blot assay was used to evaluate expres-sions of p65, p-p65, IκBα and p-IκBα. Activities of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA) contents were measured spectrophotometrically. The results demonstrated that TNF-α induced a significant increase in cell viability and inflammatory cytokines, including expressions of Interleukin (IL)-6, IL-8, IL-22 and IL-1β in HaCaT cells, which was dose-dependently inhibited by kirenol. Similarly, TNF-α-induced cell migration was also suppressed by kirenol treatment. Furthermore, TNF-α stimuli induced the upregulation of phosphorylation levels of p65 and IκBα as well as p-p65–p65 and p-IκBα–IκBα ratios, whereas kirenol significantly suppressed the activation of cellular nuclear factor-kappa B (NF-κB) signaling pathway. In addition, kirenol significantly decreased the level of MDA but increased the levels of SOD, CAT and GSH in a dose-dependent manner. These results proposed that kirenol could inhibit the proliferation, migration, expression of inflammatory factors, and oxidative stress in HaCaT cells via suppressing NF-κB signaling pathway.
{"title":"Kirenol inhibits TNF-α-induced proliferation and migration of HaCaT cells by regulating NF-κB pathway","authors":"Jin Li, Fang Ren, Wenliang Yan, H. Sang","doi":"10.15586/qas.v13i4.968","DOIUrl":"https://doi.org/10.15586/qas.v13i4.968","url":null,"abstract":"Psoriasis is a common chronic, inflammatory skin disease possessing properties of inflammatory cell infiltration and excessive proliferation of keratinocytes, the occurrence and development of which remain fully elucidated. Therefore, the study was designed to determine the effects of kirenol (50, 100 and 200 μg/mL) on Cultured Human Keratinocytes (cells) (HaCaT) in vitro and reveal its molecular mechanism. The in vitro psoriasis model was established utilizing tumor necrosis factor-α (TNF-α)-stimulated HaCaT cells. Kirenol, a diterpenoid compound, was applied at different concentrations (50, 100 and 200 μg/mL) to HaCaT cells for 24 h. The Cell Counting Kit-8 (CCK-8) and thymidine monobromodeoxyuridine (BrdU) assays were used to assess cell viability and proliferation, followed by assessment of cell migration by Transwell assay. Subsequently, inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA), and Western blot assay was used to evaluate expres-sions of p65, p-p65, IκBα and p-IκBα. Activities of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA) contents were measured spectrophotometrically. The results demonstrated that TNF-α induced a significant increase in cell viability and inflammatory cytokines, including expressions of Interleukin (IL)-6, IL-8, IL-22 and IL-1β in HaCaT cells, which was dose-dependently inhibited by kirenol. Similarly, TNF-α-induced cell migration was also suppressed by kirenol treatment. Furthermore, TNF-α stimuli induced the upregulation of phosphorylation levels of p65 and IκBα as well as p-p65–p65 and p-IκBα–IκBα ratios, whereas kirenol significantly suppressed the activation of cellular nuclear factor-kappa B (NF-κB) signaling pathway. In addition, kirenol significantly decreased the level of MDA but increased the levels of SOD, CAT and GSH in a dose-dependent manner. These results proposed that kirenol could inhibit the proliferation, migration, expression of inflammatory factors, and oxidative stress in HaCaT cells via suppressing NF-κB signaling pathway.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47720061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The purpose of this study was to investigate the therapeutic effects of picroside II on diabetic nephropathy and reveal the involved underlying signal pathway. Male Sprague–Dawley (SD) mice were used to construct an animal model of streptozotocin (STZ)-induced diabetic nephropathy. Body weight and fasting blood glucose values were recorded. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of proteinuria, blood urea nitrogen (BUN), serum creatinine (Scr), interleukin (IL)-1β, IL-6, monocyte chemoattractant protein-1 (MCP-1) and necrosis factor alpha (TNF-α). Protein expression was determined using Western blotting test. Hema-toxylin and eosin (H&E) staining was used to examine the morphological changes in kidney tissues. Treatment with picroside II (10 and 20 mg/kg) increased the STZ-induced reduction in body weight of diabetic mice. It also reversed the elevation of fasting blood glucose in STZ-induced diabetic mice. The levels of proteinuria, BUN and Scr were significantly increased in STZ-induced diabetic mice and these increments were prevented by picroside II. The serum levels of MCP-1, IL-1β, IL-6 and TNF-α were reduced, and the morphological damage was lessened by Picroside II in mice with diabetic nephropathy. Besides, picroside II prevented the activation of TLR4/NF-κB pathway. This study proved that picroside II inhibited inflammatory response and prevented kidney injury in mice with diabetic nephropathy through modulation of TLR4/NF-κB pathway, indicating beneficial effect of picroside II on diabetic nephropathy.
{"title":"Picroside II prevents inflammation injury in mice with diabetic nephropathy via TLR4/NF-κB pathway","authors":"Chunmei Ma, Aijie Shi","doi":"10.15586/qas.v13i4.984","DOIUrl":"https://doi.org/10.15586/qas.v13i4.984","url":null,"abstract":"The purpose of this study was to investigate the therapeutic effects of picroside II on diabetic nephropathy and reveal the involved underlying signal pathway. Male Sprague–Dawley (SD) mice were used to construct an animal model of streptozotocin (STZ)-induced diabetic nephropathy. Body weight and fasting blood glucose values were recorded. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of proteinuria, blood urea nitrogen (BUN), serum creatinine (Scr), interleukin (IL)-1β, IL-6, monocyte chemoattractant protein-1 (MCP-1) and necrosis factor alpha (TNF-α). Protein expression was determined using Western blotting test. Hema-toxylin and eosin (H&E) staining was used to examine the morphological changes in kidney tissues. Treatment with picroside II (10 and 20 mg/kg) increased the STZ-induced reduction in body weight of diabetic mice. It also reversed the elevation of fasting blood glucose in STZ-induced diabetic mice. The levels of proteinuria, BUN and Scr were significantly increased in STZ-induced diabetic mice and these increments were prevented by picroside II. The serum levels of MCP-1, IL-1β, IL-6 and TNF-α were reduced, and the morphological damage was lessened by Picroside II in mice with diabetic nephropathy. Besides, picroside II prevented the activation of TLR4/NF-κB pathway. This study proved that picroside II inhibited inflammatory response and prevented kidney injury in mice with diabetic nephropathy through modulation of TLR4/NF-κB pathway, indicating beneficial effect of picroside II on diabetic nephropathy.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41345881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elevated reactive oxygen species (ROS) induce oxidative damage in retinal pigment epithelium (RPE) and con-tribute to the development of age-related macular degeneration (AMD). Gastrodin plays an antioxidant role in distinct diseases, such as epilepsy, cerebral ischemia, Alzheimer’s disease, and cardiovascular diseases. However, the function of gastrodin in AMD remains unclear. Human RPE (ARPE-19) cells were incubated with 300 μM hydrogen peroxide (H2O2) for 24 hours. The results showed that H2O2 decreased cell viability and promoted the cell apoptosis of ARPE-19 cells. H2O2-induced ARPE-19 cells were then treated with different concentrations of gastrodin. Gastrodin increased cell viability of H2O2-induced ARPE-19 cells, suppressed the cell apoptosis of H2O2-induced ARPE-19 cells with reduced B-cell lymphoma (Bcl)-2 like protein (Bax), and enhanced Bcl-2. The levels of ROS were enhanced, malondialdehyde (MDA) was up-regulated, and superoxide dismutase (SOD) and glutathione (GSH) were down-regulated in H2O2-induced ARPE-19 cells. However, gastrodin reduced the lev-els of ROS and MDA and elevated SOD and GSH in H2O2-induced ARPE-19 cells. Furthermore, H2O2-induced increase of inducible nitric oxide synthase (iNOS) and p-p38 proteins in ARPE-19 was reversed by gastrodin. In conclusion, gastrodin exerted antiapoptotic and antioxidant capacities to protect against H2O2-induced oxidative stress in RPE, thereby acting as a potential agent for managing AMD.
{"title":"Gastrodin represses hydrogen peroxide-induced oxidative stress in retinal pigment epithelial cells through p38MAPK/iNOS pathway","authors":"X. Zhou, Ximing Zhao","doi":"10.15586/qas.v13i4.969","DOIUrl":"https://doi.org/10.15586/qas.v13i4.969","url":null,"abstract":"Elevated reactive oxygen species (ROS) induce oxidative damage in retinal pigment epithelium (RPE) and con-tribute to the development of age-related macular degeneration (AMD). Gastrodin plays an antioxidant role in distinct diseases, such as epilepsy, cerebral ischemia, Alzheimer’s disease, and cardiovascular diseases. However, the function of gastrodin in AMD remains unclear. Human RPE (ARPE-19) cells were incubated with 300 μM hydrogen peroxide (H2O2) for 24 hours. The results showed that H2O2 decreased cell viability and promoted the cell apoptosis of ARPE-19 cells. H2O2-induced ARPE-19 cells were then treated with different concentrations of gastrodin. Gastrodin increased cell viability of H2O2-induced ARPE-19 cells, suppressed the cell apoptosis of H2O2-induced ARPE-19 cells with reduced B-cell lymphoma (Bcl)-2 like protein (Bax), and enhanced Bcl-2. The levels of ROS were enhanced, malondialdehyde (MDA) was up-regulated, and superoxide dismutase (SOD) and glutathione (GSH) were down-regulated in H2O2-induced ARPE-19 cells. However, gastrodin reduced the lev-els of ROS and MDA and elevated SOD and GSH in H2O2-induced ARPE-19 cells. Furthermore, H2O2-induced increase of inducible nitric oxide synthase (iNOS) and p-p38 proteins in ARPE-19 was reversed by gastrodin. In conclusion, gastrodin exerted antiapoptotic and antioxidant capacities to protect against H2O2-induced oxidative stress in RPE, thereby acting as a potential agent for managing AMD.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67104744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human dental pulp stem cells (hDPSCs) are capable of forming mineralized nodules. The proliferation and osteogenic differentiation of hDPSCs are very important for alleviating tooth defects caused by related diseases. Angel-ica polysaccharide (ASP) is the main bioactive ingredient extracted from the angelica root. ASP has a variety of biological functions, including immune regulation, antitumor activity, and hematopoiesis. However, its possible effects on hDPSCs are still unclear. In this study, we aimed to investigate the role of ASP in periodontal diseases. We found that ASP promoted the proliferation of hDPSCs and osteogenic differentiation of hDPSCs. We further found that it promoted the expression of osteogenic-related genes, including ALP, RUNX2, Col1a1, and OCN. Mechanically, we found that ASP activated the Wnt/β-catenin pathway. In conclusion, our results suggested that ASP promoted the proliferation and osteogenic differentiation of hDPSCs via the Wnt/β-catenin pathway.
{"title":"Angelica sinensis polysaccharide promotes the proliferation and osteogenic differentiation of human dental pulp stem cells (hDPSCs) by activating the wnt/β-catenin pathway","authors":"Tiantian Mao, Youjian Peng, Ruobing Peng, Xiaoying Wei","doi":"10.15586/qas.v13i4.989","DOIUrl":"https://doi.org/10.15586/qas.v13i4.989","url":null,"abstract":"Human dental pulp stem cells (hDPSCs) are capable of forming mineralized nodules. The proliferation and osteogenic differentiation of hDPSCs are very important for alleviating tooth defects caused by related diseases. Angel-ica polysaccharide (ASP) is the main bioactive ingredient extracted from the angelica root. ASP has a variety of biological functions, including immune regulation, antitumor activity, and hematopoiesis. However, its possible effects on hDPSCs are still unclear. In this study, we aimed to investigate the role of ASP in periodontal diseases. We found that ASP promoted the proliferation of hDPSCs and osteogenic differentiation of hDPSCs. We further found that it promoted the expression of osteogenic-related genes, including ALP, RUNX2, Col1a1, and OCN. Mechanically, we found that ASP activated the Wnt/β-catenin pathway. In conclusion, our results suggested that ASP promoted the proliferation and osteogenic differentiation of hDPSCs via the Wnt/β-catenin pathway.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43768559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lu Gao, Yuan Hu, Meidan Sun, Xiang-feng Zheng, Ming Yang, Shengqi Rao
This study aimed to evaluate the antimicrobial efficacy of the combination of ɛ-polylysine (ɛ-PL) and carvacrol (Car) against foodborne pathogens, Escherichia coli and Staphylococcus aureus. The minimum inhibitory concentrations (MICs) of ɛ-PL (Car) against E. coli and S. aureus were 25 μg/mL (320 μg/mL) and 12.5 μg/mL (320 μg/mL), respectively. Checkerboard assays showed that the combination of ɛ-PL and Car exerted synergistic effects against E. coli and S. aureus with fraction inhibitory concentration index (FICI) of 0.375 and 0.5, respectively. It demonstrated that the combination of ɛ-PL and Car significantly inhibited the growth of the two strains compared to single treatment. Furthermore, the mode of action of ɛ-PL (6.25 μg/mL) or Car (80 μg/mL) in inhibiting E. coli and S. aureus was researched by assessing their changes with regard to cellular membrane integrity, membrane permeability, respiratory activity, and membrane structure. A combination of ɛ-PL and Car increased the damage to cell membranes and their permeability and led to the release of 260 nm absorbing materials, decreased respiratory-chain dehydrogenase activity compared with ɛ-PL or Car treatment alone. These results demonstrated that the combination of ɛ-PL and Car could be used as a new promising naturally sourced food preservative.
{"title":"Synergistic antibacterial effects of carvacrol and ε-polylysine","authors":"Lu Gao, Yuan Hu, Meidan Sun, Xiang-feng Zheng, Ming Yang, Shengqi Rao","doi":"10.15586/qas.v13i4.928","DOIUrl":"https://doi.org/10.15586/qas.v13i4.928","url":null,"abstract":"This study aimed to evaluate the antimicrobial efficacy of the combination of ɛ-polylysine (ɛ-PL) and carvacrol (Car) against foodborne pathogens, Escherichia coli and Staphylococcus aureus. The minimum inhibitory concentrations (MICs) of ɛ-PL (Car) against E. coli and S. aureus were 25 μg/mL (320 μg/mL) and 12.5 μg/mL (320 μg/mL), respectively. Checkerboard assays showed that the combination of ɛ-PL and Car exerted synergistic effects against E. coli and S. aureus with fraction inhibitory concentration index (FICI) of 0.375 and 0.5, respectively. It demonstrated that the combination of ɛ-PL and Car significantly inhibited the growth of the two strains compared to single treatment. Furthermore, the mode of action of ɛ-PL (6.25 μg/mL) or Car (80 μg/mL) in inhibiting E. coli and S. aureus was researched by assessing their changes with regard to cellular membrane integrity, membrane permeability, respiratory activity, and membrane structure. A combination of ɛ-PL and Car increased the damage to cell membranes and their permeability and led to the release of 260 nm absorbing materials, decreased respiratory-chain dehydrogenase activity compared with ɛ-PL or Car treatment alone. These results demonstrated that the combination of ɛ-PL and Car could be used as a new promising naturally sourced food preservative.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42102858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ruscogenin exerts an anti-inflammatory effect in the pathogenesis of various human diseases, including pulmonary hypertension, acute lung injury, acute pancreatitis and cerebral ischemia. Its role in isoflurane-induced rats with postoperative cognitive dysfunction (POCD) was investigated in this study. Aged rats were exposed to isoflurane for establishing a model of POCD, and administered with ruscogenin by gavage. Cognitive dysfunction was evaluated by the Morris water maze test. Hematoxylin and Eosin (H&E) staining was designed to assess neuronal damage. Markers of brain damage and neuroinflammation were detected by enzyme-linked-immunosorbent serologic assay. Isoflurane exposure caused impaired cognitive function by increasing escape latency, decreasing the time taken for crossing target and time in target quadrant. However, administration of ruscogenin reversed these cognitive dysfunctions. Abnormal morphological phenomena on neurons and enhanced levels of serum calcium-binding protein β (S-100β) and neuron-specific enolase (NSE) were identified in mice post-isoflurane exposure. Administration of ruscogenin ameliorated the neuronal morphological damages and reduced the levels of S-100β and NSE in the hippocampi of isoflurane-induced aged mice. Ruscogenin also attenuated isoflurane-induced enhancements in the levels of Interleukin (IL)-1β, IL-6 and tumor necrosis factor-alpha in the hippocampi of mice. Isoflurane-induced enhancements in the mRNA expression levels of NLR family pyrin domain containing 3 (NLRP3), ASC, IL-1β and IL-18 proteins were also restored by administration of ruscogenin. Ruscogenin exerted neuroprotective effects against isoflurane-induced cognitive dysfunction and neuroinflammation through blocking of NLRP3 pathway.
{"title":"Ruscogenin alleviates cognitive dysfunction by inhibiting the activation of isoflurane-induced NLRP3 inflammasome in aged mice","authors":"X. Liang, Xiao-Lin Luo, Dan-Dan Li, Ling-Zu Kong","doi":"10.15586/qas.v13i3.964","DOIUrl":"https://doi.org/10.15586/qas.v13i3.964","url":null,"abstract":"Ruscogenin exerts an anti-inflammatory effect in the pathogenesis of various human diseases, including pulmonary hypertension, acute lung injury, acute pancreatitis and cerebral ischemia. Its role in isoflurane-induced rats with postoperative cognitive dysfunction (POCD) was investigated in this study. Aged rats were exposed to isoflurane for establishing a model of POCD, and administered with ruscogenin by gavage. Cognitive dysfunction was evaluated by the Morris water maze test. Hematoxylin and Eosin (H&E) staining was designed to assess neuronal damage. Markers of brain damage and neuroinflammation were detected by enzyme-linked-immunosorbent serologic assay. Isoflurane exposure caused impaired cognitive function by increasing escape latency, decreasing the time taken for crossing target and time in target quadrant. However, administration of ruscogenin reversed these cognitive dysfunctions. Abnormal morphological phenomena on neurons and enhanced levels of serum calcium-binding protein β (S-100β) and neuron-specific enolase (NSE) were identified in mice post-isoflurane exposure. Administration of ruscogenin ameliorated the neuronal morphological damages and reduced the levels of S-100β and NSE in the hippocampi of isoflurane-induced aged mice. Ruscogenin also attenuated isoflurane-induced enhancements in the levels of Interleukin (IL)-1β, IL-6 and tumor necrosis factor-alpha in the hippocampi of mice. Isoflurane-induced enhancements in the mRNA expression levels of NLR family pyrin domain containing 3 (NLRP3), ASC, IL-1β and IL-18 proteins were also restored by administration of ruscogenin. Ruscogenin exerted neuroprotective effects against isoflurane-induced cognitive dysfunction and neuroinflammation through blocking of NLRP3 pathway.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45777468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The aim of this study was to investigate the protective role of Juglanin in rats suffering from acute myocardial infarction (AMI). Male Sprague–Dawley (SD) mice were used to construct the AMI model. Hematoxylin and Eosin staining was used to observe the morphological changes of cardiomyocytes. Changes in lactate dehydro-genase (LDH), caspase-3 and caspase-9 were measured using commercial kits. Enzyme-linked immunosorbent assay was used to measure the serum level of creatine kinase myocardial band (CK-MB), Interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), IL-10 and IL-1β. Protein expression and phosphorylation were determined by Western blotting test. The morphology of cardiomyocytes suffered great changes because of AMI, which included focal myocardial necrosis, severe inflammatory cell infiltration, and myocardial fiber dissolution, disorder, and partial rupture. The morphological changes in cardiomyocytes were significantly ameliorated through treatment with Juglanin (10 mg/kg and 30 mg/kg). Increment of serum CK-MB, LDH, IL-6, TNF-α, IL-10 and IL-1β was reduced in AMI rats treated with 10-mg/kg and 30-mg/kg Juglanin. Cell apoptosis was also inhibited by Juglanin treatment. AMI-induced phosphorylation of p38, extracellular signal-regulated kinase (p-ERK) and c-Jun N-terminal kinase (p-JNK) was suppressed through treatment with Juglanin. This study demonstrated that Juglanin alleviated myocardial injury in rats because of AMI through inactivation of mitogen-activated protein kinase signaling pathway, thus indicating a protective role in rat AMI model.
{"title":"Juglanin alleviates myocardial injury in rats with acute myocardial infarction through modulating MAPK signaling pathway","authors":"Jing Sun, Lei Song","doi":"10.15586/qas.v13i3.983","DOIUrl":"https://doi.org/10.15586/qas.v13i3.983","url":null,"abstract":"The aim of this study was to investigate the protective role of Juglanin in rats suffering from acute myocardial infarction (AMI). Male Sprague–Dawley (SD) mice were used to construct the AMI model. Hematoxylin and Eosin staining was used to observe the morphological changes of cardiomyocytes. Changes in lactate dehydro-genase (LDH), caspase-3 and caspase-9 were measured using commercial kits. Enzyme-linked immunosorbent assay was used to measure the serum level of creatine kinase myocardial band (CK-MB), Interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), IL-10 and IL-1β. Protein expression and phosphorylation were determined by Western blotting test. The morphology of cardiomyocytes suffered great changes because of AMI, which included focal myocardial necrosis, severe inflammatory cell infiltration, and myocardial fiber dissolution, disorder, and partial rupture. The morphological changes in cardiomyocytes were significantly ameliorated through treatment with Juglanin (10 mg/kg and 30 mg/kg). Increment of serum CK-MB, LDH, IL-6, TNF-α, IL-10 and IL-1β was reduced in AMI rats treated with 10-mg/kg and 30-mg/kg Juglanin. Cell apoptosis was also inhibited by Juglanin treatment. AMI-induced phosphorylation of p38, extracellular signal-regulated kinase (p-ERK) and c-Jun N-terminal kinase (p-JNK) was suppressed through treatment with Juglanin. This study demonstrated that Juglanin alleviated myocardial injury in rats because of AMI through inactivation of mitogen-activated protein kinase signaling pathway, thus indicating a protective role in rat AMI model.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44545169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Naqash, H. Naik, S. Z. Hussain, H. Makroo, B. N. Dar
Onion paste is a commercially used processed product that reduces cooking time. Industrial processing of onion paste involves various treatments that affect the overall nutritional profile of the final product. In this study, effect of various thermal treatment conditions was evaluated, with temperature and time ranging between 70 and 90°C for 8 to 22 min, respectively. Changes in quercetin, pyruvic acid, and quality characteristics of fresh onion paste were investigated. A negative linear trend was observed in quercetin, pyruvic acid, viscosity, ascorbic acid, and total plate count, with an increase in temperature and time. An interactive and combined effect of time and tem-perature showed a positive linear relationship with color difference. For all the quality parameters investigated in this study, thermal treatment at 87°C for 15 min was found to be optimum for development of shelf-stable onion paste. Quercetin and pyruvic acid content were found to be 2.587±0.03 g kg–1 and 0.086±0.004 µmol kg–1, respectively. Optimum conditions depicted better retention of principal compounds as compared to the other experimental conditions and exhibited safer quality product as compared to the untreated sample.Industrial relevance: Brown Spanish onion is a perishable produce due to high moisture content. In order to reduce its postharvest losses at domestic and commercial levels, optimized processing parameters for the production of onion paste can be economically beneficial, and it is a highly acclaimed product for consumer usage.
洋葱酱是一种商业上使用的加工产品，可以减少烹饪时间。洋葱酱的工业加工涉及各种处理，这些处理会影响最终产品的整体营养状况。在本研究中，评估了不同热处理条件的效果，温度和时间分别在70 - 90℃之间，分别为8 - 22 min。研究了新鲜洋葱酱中槲皮素、丙酮酸的变化及其品质特性。槲皮素、丙酮酸、黏度、抗坏血酸和总平板数随温度和时间的增加呈负线性趋势。时间和温度的交互和联合作用与色差呈线性正相关。在本研究中考察的所有质量参数中，87°C 15分钟的热处理被发现是最适合货架稳定的洋葱酱的发展。槲皮素和丙酮酸含量分别为2.587±0.03 g kg-1和0.086±0.004µmol kg-1。与其他实验条件相比，最佳条件可以更好地保留主要化合物，并且与未经处理的样品相比，显示出更安全的质量产品。工业相关性:棕色西班牙洋葱是一种易腐烂的产品，由于高水分含量。为了减少国内和商业层面的采后损失，对洋葱酱的生产工艺参数进行了优化，具有经济效益，是深受消费者好评的产品。
{"title":"Effect of thermal treatment on physicochemical, phytochemical, and microbiological characteristics of brown Spanish onion paste","authors":"S. Naqash, H. Naik, S. Z. Hussain, H. Makroo, B. N. Dar","doi":"10.15586/qas.v13i4.959","DOIUrl":"https://doi.org/10.15586/qas.v13i4.959","url":null,"abstract":"Onion paste is a commercially used processed product that reduces cooking time. Industrial processing of onion paste involves various treatments that affect the overall nutritional profile of the final product. In this study, effect of various thermal treatment conditions was evaluated, with temperature and time ranging between 70 and 90°C for 8 to 22 min, respectively. Changes in quercetin, pyruvic acid, and quality characteristics of fresh onion paste were investigated. A negative linear trend was observed in quercetin, pyruvic acid, viscosity, ascorbic acid, and total plate count, with an increase in temperature and time. An interactive and combined effect of time and tem-perature showed a positive linear relationship with color difference. For all the quality parameters investigated in this study, thermal treatment at 87°C for 15 min was found to be optimum for development of shelf-stable onion paste. Quercetin and pyruvic acid content were found to be 2.587±0.03 g kg–1 and 0.086±0.004 µmol kg–1, respectively. Optimum conditions depicted better retention of principal compounds as compared to the other experimental conditions and exhibited safer quality product as compared to the untreated sample.Industrial relevance: Brown Spanish onion is a perishable produce due to high moisture content. In order to reduce its postharvest losses at domestic and commercial levels, optimized processing parameters for the production of onion paste can be economically beneficial, and it is a highly acclaimed product for consumer usage.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44505718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Plumbagin, a bioactive phytoconstituent, is isolated from the root of Plumbago zeylanica L. Plumbagin pos-sesses antidiabetic effect to mediate glucose homeostasis, wound healing and diabetic nephropathy. However, the involvement of plumbagin in gestational diabetes mellitus (GDM) has not been reported yet. Trophoblast cell line (HTR8/SVneo) was incubated with high glucose to establish cell model of GDM. Cell viability and proliferation were detected by MTT and EdU staining. Flow cytometry was used to investigate cell apoptosis. Cell viability of HTR8/SVneo was reduced by high glucose or incubation of plumbagin. Plumbagin restored reduced cell viability and proliferation of HTR8/SVneo induced by high glucose. Plumbagin attenuated high glucose-induced cell apoptosis in HTR8/SVneo cells through upregulation of Bcl-2 and down-regulation of Bax, cleaved caspase-3 and cleaved caspase-9. Protein expression of glucose transporter type 4 (GLUT-4), insulin receptor (INSR)-B and INSR substrate (IRS1) was decreased in high glucose-induced HTR8/SVneo but increased by plumbagin. The suppressive effects of high glucose on phosphorylation of AKT and mTOR in HTR8/SVneo were reversed by plumbagin. Plumbagin improved high glucose-induced cell apoptosis and insulin resistance of HTR8/SVneo through activation of AKT/mTOR pathway, suggesting that plumbagin might be used as a potential strategy for the prevention of GDM.
{"title":"Plumbagin attenuates high glucose-induced trophoblast cell apoptosis and insulin resistance via activating AKT/mTOR pathway","authors":"Yilin Zhang, Guantai Ni, Hongying Yang","doi":"10.15586/qas.v13i3.960","DOIUrl":"https://doi.org/10.15586/qas.v13i3.960","url":null,"abstract":"Plumbagin, a bioactive phytoconstituent, is isolated from the root of Plumbago zeylanica L. Plumbagin pos-sesses antidiabetic effect to mediate glucose homeostasis, wound healing and diabetic nephropathy. However, the involvement of plumbagin in gestational diabetes mellitus (GDM) has not been reported yet. Trophoblast cell line (HTR8/SVneo) was incubated with high glucose to establish cell model of GDM. Cell viability and proliferation were detected by MTT and EdU staining. Flow cytometry was used to investigate cell apoptosis. Cell viability of HTR8/SVneo was reduced by high glucose or incubation of plumbagin. Plumbagin restored reduced cell viability and proliferation of HTR8/SVneo induced by high glucose. Plumbagin attenuated high glucose-induced cell apoptosis in HTR8/SVneo cells through upregulation of Bcl-2 and down-regulation of Bax, cleaved caspase-3 and cleaved caspase-9. Protein expression of glucose transporter type 4 (GLUT-4), insulin receptor (INSR)-B and INSR substrate (IRS1) was decreased in high glucose-induced HTR8/SVneo but increased by plumbagin. The suppressive effects of high glucose on phosphorylation of AKT and mTOR in HTR8/SVneo were reversed by plumbagin. Plumbagin improved high glucose-induced cell apoptosis and insulin resistance of HTR8/SVneo through activation of AKT/mTOR pathway, suggesting that plumbagin might be used as a potential strategy for the prevention of GDM.","PeriodicalId":20868,"journal":{"name":"Quality Assurance and Safety of Crops & Foods","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2021-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49255982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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